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Human GADD45B Protein expressed in Escherichia coli (E. coli) - ABIN666871
Takekawa, Saito: A family of stress-inducible GADD45-like proteins mediate activation of the stress-responsive MTK1/MEKK4 MAPKKK. in Cell 1998
Show all 2 references for ABIN666871
investigated the functional effects of Coiled-Coil Domain Containing 80-loss-of-function during embryonic development and verified its interaction with gadd45beta2 in somitogenesis
regulated expression of gadd45beta genes in the anterior PSM is required for somite segmentation.
This study indicates that PPAR alpha (show PPARA Proteins) activation drives demethylation of the CpG islands of the Gadd45b promoter in the mouse liver and that epigenetic change at the Gadd45b promoter is critical for Gadd45b induction.
Data suggest that the increased expression of Gadd45beta induced by repeated administration of L-DOPA may be beneficial in patients with Parkinson's disease.
lower nucleus accumbens levels may affect Bdnf (show BDNF Proteins) expression possibly leading to altered alcohol-drinking behavior
Gadd45b mediates the action of electroconvulsive shock-induced neural stem cell proliferation in the hippocampus.
Results suggest the possibility that differential Gadd45a (show GADD45A Proteins), Gadd45b and Gadd45g (show GADD45G Proteins) expression during development affects neurons, contributing cortical evolution and diversity
Hepatic oxidative stress activates the Gadd45b gene by way of degradation of the transcriptional repressor STAT3 (show STAT3 Proteins).
Modulation of the TGFbeta (show TGFB1 Proteins)/NFkappaB/Gadd45b signaling pathway may provide a means to enhance the neuroprotective effect of Gadd45b in RGCs.
These results implicate Gadd45b as a learning-induced gene and a regulator of memory formation and are consistent with its potential role in active DNA demethylation in memory.
The data suggest that GADD45beta plays a complex role in regulating adaptive immunity and, depending on the model, either enhances or suppresses inflammation.
The current studies suggest that Gadd45b may be important for long-term hippocampus-dependent memory storage.
We used a new approach to search for human genes repressed by small nucleic acids (microRNAs) expressed by a gammaherpesvirus (KSHV), which identified a gene called GADD45B as a target of microRNAs. Repression of GADD45B, which is expressed in response to DNA damage, benefited survival of infected cells in response to a DNA damage response. This information could be used to design new treatments for herpesvirus infections
Gadd45beta could be a suitable biomarker of cardiomyocytes apoptosis in newborns experiencing hypoxia in the first day of life, as its highest tissue immunoexpression around at the first six hours after birth.
Nrf2 (show GABPA Proteins)-Gadd45b signaling axis exhibited a protective role in antimony trioxide-induced cell apoptosis.
our data demonstrate that C/EBPbeta (show CEBPB Proteins) plays a central role in controlling Gadd45beta gene expression in articular chondrocytes
The gadd45b gene has both tumor suppressor and tumor promoter functions, dependent on the tissue/cell type and transforming event. (Review)
Gadd45B protects the liver through two entirely different processes: binding MKK7 (show MAP2K7 Proteins) to block damaging signal transduction or binding CAR to coactivate anabolic transcription. (Review)
as such may play an unappreciated role in tumorigenesis. The exact mechanism of GADD45B inactivation and overexpression requires further investigation. GADD45B could be a potential therapeutic target for CRC (show CALR Proteins) treatment in future
Cadmium chloride can induce DNA damage and increase expression levels of the gadd153 (show DDIT3 Proteins) and gadd45beta promoters in HepG2 cells.
finding show there is an increased expression and decreased promoter binding of GADD45b in psychotic subjects.
GADD45beta is a novel pituitary tumor suppressor whose reexpression blocks proliferation, survival, and tumorigenesis
This gene is a member of a group of genes whose transcript levels are increased following stressful growth arrest conditions and treatment with DNA-damaging agents. The genes in this group respond to environmental stresses by mediating activation of the p38/JNK pathway. This activation is mediated via their proteins binding and activating MTK1/MEKK4 kinase, which is an upstream activator of both p38 and JNK MAPKs. The function of these genes or their protein products is involved in the regulation of growth and apoptosis. These genes are regulated by different mechanisms, but they are often coordinately expressed and can function cooperatively in inhibiting cell growth.
, growth arrest and DNA damage 45 beta
, Myeloid differentiation primary response protein MyD118
, growth arrest and DNA damage-inducible protein GADD45 beta
, growth arrest and DNA-damage-inducible protein GADD45 beta
, myeloid differentiation primary response gene 118
, myeloid differentiation primary response protein MyD118
, negative growth regulatory protein MyD118
, myeloid differentiation primary response
, growth arrest and DNA-damage-inducible 45 beta